BACKGROUND: Premature ventricular complexes (PVCs) and ventricular tachycardia (VT) are associated with persistent symptoms and ventricular dysfunction. Approved medical therapies have undesirable side effects and proarrhythmic liability. Ranolazine is a novel antianginal that preferentially blocks the late sodium current. This current is enhanced among patients with cardiomyopathy; a promising target population for ranolazine. The utility of ranolazine, however, for ventricular arrhythmia suppression has not been well characterized. OBJECTIVES: We sought to determine the effectiveness of ranolazine for suppression of ventricular ectopy, particularly in the setting of ventricular dysfunction where enhanced efficacy might be expected. METHODS: We retrospectively evaluated eight patients (six with >10% PVC burden and two with incessant VT) treated with ranolazine. Arrhythmia frequency was evaluated by continuous monitoring before and after ranolazine initiation and the correlation between ventricular function and reduction in PVC burden was assessed. RESULTS: Among six patients with PVCs, ranolazine resulted in a median decrease in PVC burden of 60.2% (P = 0.06). In two cases of apparent PVC-induced cardiomyopathy, normalization of ventricular function was observed. A significant, inverse correlation between baseline ejection fraction and percentage reduction in PVCs was observed (rho = -0.89, P = 0.02). In two patients treated for incessant VT despite Class III antiarrhythmic therapy, ranolazine eliminated VT and prevented recurrent defibrillator therapy. CONCLUSIONS: Although not approved for this indication, ranolazine appears effective for symptomatic ventricular arrhythmias. The reduction in PVC burden was greatest among individuals with reduced ventricular function, perhaps due to enhanced late sodium current associated with cardiomyopathy. A confirmatory prospective trial seems warranted.
BACKGROUND: Premature ventricular complexes (PVCs) and ventricular tachycardia (VT) are associated with persistent symptoms and ventricular dysfunction. Approved medical therapies have undesirable side effects and proarrhythmic liability. Ranolazine is a novel antianginal that preferentially blocks the late sodium current. This current is enhanced among patients with cardiomyopathy; a promising target population for ranolazine. The utility of ranolazine, however, for ventricular arrhythmia suppression has not been well characterized. OBJECTIVES: We sought to determine the effectiveness of ranolazine for suppression of ventricular ectopy, particularly in the setting of ventricular dysfunction where enhanced efficacy might be expected. METHODS: We retrospectively evaluated eight patients (six with >10% PVC burden and two with incessant VT) treated with ranolazine. Arrhythmia frequency was evaluated by continuous monitoring before and after ranolazine initiation and the correlation between ventricular function and reduction in PVC burden was assessed. RESULTS: Among six patients with PVCs, ranolazine resulted in a median decrease in PVC burden of 60.2% (P = 0.06). In two cases of apparent PVC-induced cardiomyopathy, normalization of ventricular function was observed. A significant, inverse correlation between baseline ejection fraction and percentage reduction in PVCs was observed (rho = -0.89, P = 0.02). In two patients treated for incessant VT despite Class III antiarrhythmic therapy, ranolazine eliminated VT and prevented recurrent defibrillator therapy. CONCLUSIONS: Although not approved for this indication, ranolazine appears effective for symptomatic ventricular arrhythmias. The reduction in PVC burden was greatest among individuals with reduced ventricular function, perhaps due to enhanced late sodium current associated with cardiomyopathy. A confirmatory prospective trial seems warranted.
Authors: Etienne M Aliot; William G Stevenson; Jesus Ma Almendral-Garrote; Frank Bogun; C Hugh Calkins; Etienne Delacretaz; Paolo Della Bella; Gerhard Hindricks; Pierre Jaïs; Mark E Josephson; Josef Kautzner; G Neal Kay; Karl-Heinz Kuck; Bruce B Lerman; Francis Marchlinski; Vivek Reddy; Martin-Jan Schalij; Richard Schilling; Kyoko Soejima; David Wilber Journal: Heart Rhythm Date: 2009-06 Impact factor: 6.343
Authors: Timir S Baman; Dave C Lange; Karl J Ilg; Sanjaya K Gupta; Tzu-Yu Liu; Craig Alguire; William Armstrong; Eric Good; Aman Chugh; Krit Jongnarangsin; Frank Pelosi; Thomas Crawford; Matthew Ebinger; Hakan Oral; Fred Morady; Frank Bogun Journal: Heart Rhythm Date: 2010-03-27 Impact factor: 6.343
Authors: Benjamin M Scirica; David A Morrow; Hanoch Hod; Sabina A Murphy; Luiz Belardinelli; Chester M Hedgepeth; Peter Molhoek; Freek W A Verheugt; Bernard J Gersh; Carolyn H McCabe; Eugene Braunwald Journal: Circulation Date: 2007-09-05 Impact factor: 29.690
Authors: Arthur J Moss; Claudio Schuger; Christopher A Beck; Mary W Brown; David S Cannom; James P Daubert; N A Mark Estes; Henry Greenberg; W Jackson Hall; David T Huang; Josef Kautzner; Helmut Klein; Scott McNitt; Brian Olshansky; Morio Shoda; David Wilber; Wojciech Zareba Journal: N Engl J Med Date: 2012-11-06 Impact factor: 91.245
Authors: Drayton A Hammond; Carmen Smotherman; Christopher A Jankowski; Stephen Tan; Omeni Osian; Dale Kraemer; Marci DeLosSantos Journal: Clin Res Cardiol Date: 2014-11-22 Impact factor: 5.460
Authors: Anja Schade; Karin Nentwich; Patrick Müller; Joachim Krug; Sebastian Kerber; Thomas Deneke Journal: Herzschrittmacherther Elektrophysiol Date: 2014-06
Authors: Lennart J de Vries; Mihran Martirosyan; Ron T van Domburg; Sip A Wijchers; Tamas Géczy; Tamas Szili-Torok Journal: J Interv Card Electrophysiol Date: 2018-01-05 Impact factor: 1.900